# name
Decreased Doublecortin (DCX) immunoreactivity in hippocampus after profound sensorineural hearing loss and vestibular dysfunction in adult mice

# metadata.dc.description.abstract[].value
Objective: sensorineural hearing loss (SNHL) and bilateral vestibulopathy (BV) have been associated with cognitive decline and incident dementia. Our aim was to investigate the combined effect of profound SNHL and BV on spatial cognition and hippocampal neurogenesis in adult mice. Methods: Single oral intake of allylnitrile produces otovestibular failure in less than a week. Behavioral assessment included recording of spontaneous activity, motor activity, spatial cognition, etc. Evaluation of hippocampal neurogenesis was performed 8 weeks after treatment by quantification of neural precursor cells and proliferating cells in the dentate gyrus by staining with doublecortin (Dcx) and Ki67, respectively. Results: Profound SNHL and BV were confirmed in the allylnitrile-treated mice respectively by means of auditory brainstem response (ABR) and acoustic startle response, and several vestibular tests. Spatial cognitive deficits, i.e. higher latency to target, were observed with the Barnes maze. In the right hemisphere, no statistically significant difference was observed between groups. In the left hemisphere, the difference in mean cell densities of Dcx positive cells was statistically significant when compared to the control group, whereas the difference in mean cell density of Ki67 positive cells did not differ significantly. Conclusion: Spatial cognitive deficits and decreased immunoreactivity to DCX in the left hippocampus were observed 8 weeks after adult mice acquired profound SNHL and BV.

# metadata.dc.rights[].value
cc by (c) Rompaey, Vincent Van et al, 2021

# metadata.dc.source[].value
Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))

# metadata.dc.title[].value
Decreased Doublecortin (DCX) immunoreactivity in hippocampus after profound sensorineural hearing loss and vestibular dysfunction in adult mice